Wakisaka Keiko Tsuji, Ichiyanagi Kenji, Ohno Seiko, Itoh Masanobu
1Department of Applied Biology, Kyoto Institute of Technology, Hashigamicyo Matsugasaki, Sakyo-ku, Kyoto, 606-8585 Japan.
2Laboratory of Genome and Epigenome Dynamics, Department of Applied Molecular Biosciences, Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, 464-8601 Japan.
Mob DNA. 2018 Feb 6;9:7. doi: 10.1186/s13100-018-0110-y. eCollection 2018.
-element transposition in the genome causes P-M hybrid dysgenesis in . Maternally deposited piRNAs suppress -element transposition in the progeny, linking them to P-M phenotypes; however, the role of zygotic piRNAs derived from paternal elements is poorly understood.
To elucidate the molecular basis of -element suppression by zygotic factors, we investigated the genomic constitution and -element piRNA production derived from fathers. As a result, we characterized males of naturally derived Q, M' and P strains, which show different capacities for the -element mobilizations introduced after hybridizations with M-strain females. The amounts of piRNAs produced in ovaries of F1 hybrids varied among the strains and were influenced by the characteristics of the piRNA clusters that harbored the elements. Importantly, while both the Q- and M'-strain fathers restrict the -element mobilization in ovaries of their daughters, the Q-strain fathers supported the production of the highest piRNA expression in the ovaries of their daughters, and the M' strain carries elements in transcriptionally active regions directing the highest expression of elements in their daughters. Interestingly, the zygotic -element piRNAs, but not the element mRNA, contributed to the variations in transposition immunity in the granddaughters.
The piRNA-cluster-embedded elements and the transcriptionally active elements from the paternal genome are both important suppressors of element activities that are co-inherited by the progeny. Expression levels of the -element piRNA and -element mRNA vary among F1 progeny due to the constitution of the paternal genome, and are involved in phenotypic variation in the subsequent generation.
基因组中的 - 元件转座会在 中导致P - M杂种不育。母本沉积的piRNA会抑制子代中的 - 元件转座，将它们与P - M表型联系起来；然而，源自父本 元件的合子piRNA的作用却知之甚少。
为了阐明合子因子对 - 元件抑制的分子基础，我们研究了源自父亲的基因组构成和 - 元件piRNA的产生。结果，我们对天然衍生的Q、M'和P品系的雄性进行了表征，这些品系在与M品系雌性杂交后引入的 - 元件动员能力不同。F1杂种卵巢中产生的piRNA数量在不同品系间有所差异，并受到含有 元件的piRNA簇特征的影响。重要的是，虽然Q品系和M'品系的父亲都限制其女儿卵巢中的 - 元件动员，但Q品系的父亲支持其女儿卵巢中piRNA表达最高，而M'品系的 元件位于转录活性区域，导致其女儿中 元件的表达最高。有趣的是，合子 - 元件piRNA而非 元件mRNA导致了孙女中 转座免疫的差异。
嵌入piRNA簇的 元件和来自父本基因组的转录活性 元件都是 元件活性的重要抑制因子，可由子代共同遗传。由于父本基因组的构成， - 元件piRNA和 - 元件mRNA的表达水平在F1后代中有所不同，并参与了后代的表型变异。
